Researchers find links between birth month and health .


health, birth month, season of birth, birth in may, health of the baby, health at birth, birth in october, disease risk

New York City medical databases and found 55 diseases that correlated with the season of birth.

People born in May have the lowest disease risk, and those in October have the highest risk, a computational method developed by scientists to investigate the relationship between birth month and disease risk shows.

“This data could help scientists uncover new disease risk factors,” said study senior author Nicholas Tatonetti, assistant professor of biomedical informatics at Columbia University Medical Center (CUMC).

Earlier research on individual diseases such as ADHD and asthma suggested a connection between birth season and incidence, but no large-scale studies had been undertaken.

The scientists compared 1,688 diseases against the birth dates and medical histories of 1.7 million patients treated at NewYork-Presbyterian Hospital/CUMC between 1985 and 2013.

The study confirmed 39 links previously reported in the medical literature.

“It’s important not to get overly nervous about these results because even though, we found significant associations the overall disease risk is not that great,” Tatonetti said.

“The risk related to birth month is relatively minor when compared to more influential variables like diet and exercise,” Tatonetti added.

The new data are consistent with previous research on individual diseases. Thus, the authors found that asthma risk is greatest for July and October babies.

“Faster computers and electronic health records are accelerating the pace of discovery. We are working to help doctors solve important clinical problems using this new wealth of data,” said the study’s lead author, Mary Regina Boland, a graduate student at Columbia.

 

Intuitive Control of a Powered Prosthetic Leg During Ambulation.


Importance  Some patients with lower leg amputations may be candidates for motorized prosthetic limbs. Optimal control of such devices requires accurate classification of the patient’s ambulation mode (eg, on level ground or ascending stairs) and natural transitions between different ambulation modes.

Objective  To determine the effect of including electromyographic (EMG) data and historical information from prior gait strides in a real-time control system for a powered prosthetic leg capable of level-ground walking, stair ascent and descent, ramp ascent and descent, and natural transitions between these ambulation modes.

Design, Setting, and Participants  Blinded, randomized crossover clinical trial conducted between August 2012 and November 2013 in a research laboratory at the Rehabilitation Institute of Chicago. Participants were 7 patients with unilateral above-knee (n = 6) or knee-disarticulation (n = 1) amputations. All patients were capable of ambulation within their home and community using a passive prosthesis (ie, one that does not provide external power).

Interventions  Electrodes were placed over 9 residual limb muscles and EMG signals were recorded as patients ambulated and completed 20 circuit trials involving level-ground walking, ramp ascent and descent, and stair ascent and descent. Data were acquired simultaneously from 13 mechanical sensors embedded on the prosthesis. Two real-time pattern recognition algorithms, using either (1) mechanical sensor data alone or (2) mechanical sensor data in combination with EMG data and historical information from earlier in the gait cycle, were evaluated. The order in which patients used each configuration was randomized (1:1 blocked randomization) and double-blinded so patients and experimenters did not know which control configuration was being used.

Main Outcomes and Measures  The main outcome of the study was classification error for each real-time control system. Classification error is defined as the percentage of steps incorrectly predicted by the control system.

Results  Including EMG signals and historical information in the real-time control system resulted in significantly lower classification error (mean, 7.9% [95% CI, 6.1%-9.7%]) across a mean of 683 steps (range, 640-756 steps) compared with using mechanical sensor data only (mean, 14.1% [95% CI, 9.3%-18.9%]) across a mean of 692 steps (range, 631-775 steps), with a mean difference between groups of 6.2% (95% CI, 2.7%-9.7%] (P = .01).

Conclusions and Relevance  In this study of 7 patients with lower limb amputations, inclusion of EMG signals and temporal gait information reduced classification error across ambulation modes and during transitions between ambulation modes. These preliminary findings, if confirmed, have the potential to improve the control of powered leg prostheses.

Pfizer ‘Hid Link’ Between Anti-Depressants and Birth Defects Alex Jones’ Infowars: There’s a war on for your mind!


Pharmaceutical mammoth Pfizer faces more than 1,000 lawsuits from victims who say that the company knew about the relationship between birth defects and their #1 best-selling anti-depressant. A claim that Pfizer has, of course, battled against.

Report: Pfizer ‘Hid Link’ Between Anti-Depressants and Birth Defects

Now, however, new reports have surfaced that Pfizer’s own scientific advisers were warning of the deadly link for more than a year. Something that my team told you in 2012 was already going on. According to Bloomberg:

“A Pfizer Inc. report shows a scientist warned executives last year about a potential link between the anti-depressant drug Zoloft and birth defects and recommended changes to the medication’s safety warning.
The document from a Pfizer drug-safety official might complicate the company’s efforts to fend off lawsuits brought by parents of children with malformed hearts. Pfizer has consistently rejected suggestions Zoloft caused newborn abnormalities and said Monday the document was taken out of context by lawyers suing the company.”
In other words, Pfizer likely employed a popular Big Pharma tactic: ignore any science that reveals serious side effects, and instead choose to pay some relatively meager fines for the damages. After all, paying a few million (or billion) in fines is often nothing compared to the profits from drugs like Zoloft, which rakes in around $2.9 billion per year alone.

After all, Pfizer has a familiar history with government fines. It was in 2009 when the corporation paid one of the largest health care fraud settlements of all time, shelling out $2.3 billion for “the intent to defraud or mislead” consumers with their painkiller Bextra. Again, a fine that is less than the sales of Zoloft for a single year.

As we read further down into the Bloomberg report, yet again it seems that research indicating serious side effects was simply ignored:

“Pfizer researchers also acknowledged in a 1998 report, which has been introduced into evidence in the Philadelphia trial, they’d found more than a dozen side-effect reports about babies’ birth defects for which their mothers’ Zoloft use couldn’t be ruled out as a cause.”
Sadly, this is nothing new for the mega pharmaceutical conglomerate. Eli Lilly & Co., the manufacturers of Prozac, did their best to hide the link between Prozac and increased risk of suicide for a number of years. Ultimately, it took a Harvard psychiatrist to proclaim that Americans were being treated like ‘guinea pigs’ by Eli Lilly & Co.’s Prozac for real public interest.

Will Pfizer end up paying a couple billion or less in fines for leading to an unknown number of life-threatening birth defects? It is the most likely outcome, for which the company is quite thankful. As long as they can write off the settlement loss and continue to take in the yearly profits, the company will get over it quickly.

Iran unveils remote surgery robot


Iranian scientists have unveiled the first domestically made high precision remote surgery robot.

Avicenna, specifically designed to carry out laparoscopic operations, was unveiled during Iran’s Second International Innovation and Technology Exhibition (INOTEX 2015) on Tuesday.

Avicenna remote surgery robot was unveiled at Iran's Second International Innovation and Technology Exhibition (INOTEX 2015) on June 9, 2015. (IRNA)

“This robot is an advanced remote surgery system that operates with a monitor and two robotic arms,” said Farzam Farahmand, the director of the Avicenna project.

He added that the Iranian robot can also be used “for abdominal and prostate surgery” with a surgeon controlling the arms and viewing the operation via the monitor.

“Operations carried out with this device minimize the damaging effects on the healthy tissues, reduce bleeding during the operation, and accelerate the recovery process,” he noted.

The machine has passed the animal testing stage and now requires proper licenses to start tests on human subjects, he added.

The robot, which is named after Iranian scientist Avicenna, was designed and developed in a joint project by the Sharif University of Technology and Tehran University of Medical Sciences.

Scientists find genetic signature enabling early, accurate sepsis diagnosis .


Systemic inflammation after injuries or surgery can dramatically alter the activity of thousands of genes, but a new study shows that changes in just 11 of them are enough to detect the presence or absence of accompanying infection.

Sepsis bacteria

The majority of sepsis cases are caused by bacterial infections that are best treated with antibiotics.

Investigators at the Stanford University School of Medicine have identified a pattern of gene activity that could help scientists create a blood test for quickly and accurately detecting whether patients are experiencing a deadly immune-system panic attack.

Sepsis is a whole-body inflammation syndrome set off when the immune system wildly overreacts to the presence of infectious pathogens. It is the leading cause of hospital deaths in the United States, accounting for nearly half of the total number, and is tied to the early deaths of at least 750,000 Americans each year. Its estimated annual cost to the health-care system exceeds $24 billion.

The great majority of sepsis cases are caused by bacterial rather than viral infections and are best treated with antibiotics. But antibiotics are unhelpful — and can be counterproductive — when a patient has an outwardly similar but infection-free syndrome called sterile inflammation, an intense, systemic inflammatory response to traumatic injuries, surgery, blood clots or other noninfectious causes.

“It’s critical for clinicians to diagnose sepsis accurately and quickly, because the risk of death from this condition increases with every passing hour it goes untreated,” said Purvesh Khatri, PhD, assistant professor of biomedical informatics research.

Sepsis or sterile inflammation?

In practice, distinguishing sepsis from sterile inflammation is a toss-up. Right now, the only diagnostics that can help do this are too slow or too inaccurate, or both, Khatri said. As a result, hospital clinicians are pressured to treat anybody showing signs of systemic inflammation with antibiotics. That can encourage bacterial drug resistance and, by killing off harmless bacteria in the gut, lead to colonization by pathogenic bacteria, such as Clostridium difficile.

 The inability to easily distinguish sepsis from sterile inflammation makes it tough for pharmaceutical companies to conduct clinical trials of drugs aimed at treating sepsis; patients may be mistakenly assumed to have sepsis when they in fact have sterile inflammation, and vice versa, Khatri said.

“We think we’ve got the makings of a diagnostic blood test that will allow clinicians to distinguish between these two types of inflammation,” he said.

Khatri is the senior author of the new study, published May 13 in Science Translational Medicine, in which a meta-analysis of publicly available data sets allowed him and his associates to tease out a gene-activation pattern that distinguishes septic from sterile systemic inflammation.

“We thought there might be some genes that the body turns on specifically in response to infection, and after sifting through a huge amount of data we found them,” said lead author Timothy Sweeney, MD, PhD, a postdoctoral scholar now doing a residency in general surgery at Stanford.

Numerous studies have been conducted to find differences in the activation levels of immune-response genes between infection-related inflammation and sterile inflammation. But these studies have yielded conflicting or murky results. One big reason is that both infection and noninfectious tissue trauma activate many of the same immune-system components and pathways. At the gene-activation level, the overlap is staggering: More than 80 percent of a person’s roughly 25,000 genes change their activity levels substantially, and mostly in the same direction, in response to massive inflammation, whether due to sepsis or sterile causes. That overlap obscures any easily detectable changes attributable solely to infection.

Needle in a haystack

Further confounding attempts to identify patterns of increases or decreases in gene activity is that fact that some patients are already experiencing sepsis when they’re admitted to the hospital, while others become infected during their hospital stay. So two different sepsis patients admitted at the same time may be at very different stages of a complex inflammation process.

“How do you figure out which tiny fraction of those changes was caused by infection? You’re looking for a needle in a haystack,” Khatri said.

The needle, it turns out, consists of a signature formed by consistent changes in the activity levels of a mere 11 genes amid the chaotic background of the other 20,000-plus genes whose activity levels fluctuate markedly over the course of systemic inflammation and recovery.

The Stanford sleuths analyzed a number of publicly available data sets containing results of studies that had assessed activity levels for the entire human genome in sepsis cases, as well as in cases of sterile inflammation. In all, they looked at more than 2,900 blood samples from nearly 1,600 patients in 27 different data sets containing medical information on diverse patient groups — men and women, young and old, suffering from sterile inflammation or sepsis, including patients who already had sepsis when first admitted to the hospital and patients who were diagnosed with it later — in addition to healthy control subjects.

The analysis consisted of two separate steps. First, the researchers scoured nine data sets containing more than 650 patient samples. They looked for genes whose activity uniformly and substantially increased or decreased, across all nine data sets, in patients within 24 hours of a sepsis diagnosis compared with genes from those not diagnosed with sepsis.

We were able to identify a slight bump in activity of these 11 genes in patients two to five days prior to their clinical diagnosis.

Initially, whatever signal may have been hiding in this group of samples was buried in the surrounding noise of myriad irrelevant gene-activity fluctuations. But the cacophony ceased when the scientists adjusted their analytical approach by taking into account when the patient was injured or operated on. That way, the researchers could account for the changes, following a surgery or injury, in inflammation-related gene activity over time, independent of the presence or absence of infection. Blood samples were therefore time-matched according to how soon a blood sample was drawn after the initial injury or surgery.

After this adjustment, 11 genes jumped out of the haystack as likely sepsis markers. The researchers confirmed this 11-gene signature in an additional 18 cohorts comprising in all more than 1,800 patient samples.

“We were able to identify a slight bump in activity of these 11 genes in patients two to five days prior to their clinical diagnosis,” said Khatri. That could mean getting an earlier diagnosis than can be achieved with current approaches, which is key considering the rapid rate at which sepsis mortality rises once it gets a foothold.

The gene-activation signature showed a sepsis-detecting accuracy surpassing that of methods now in use, Sweeney said. Combining the new technique with other current diagnostic methods is likely to be more accurate than using any one alone, he added.

Why white noise is so effective for sleeping and focus.


Ever had a hard time focusing or getting to sleep? Listening to white noise makes it possible to keep more focused and get to sleep more easily. But why is this white noise so effective?

White noise is like a tonic signal for your brain, which dampens its own internal system.

According to researchers the brain naturally craves sensory input. When it doesn’t get any, or when it’s blocked in some way, it can even start to make things up, making you hear and see things that aren’t there. This is similar to why people in sensory deprivation tanks tend to hallucinate; the brain is robbed of any stimulus and it creates its own. While sleeping during a quiet night, any random noise, whether it be a truck passing by, or the house creaking around you, your brain can become restless, causing you to wake up. A constant white noise gives your brain a tonic signal that dampens its own internal system, and allows it to shut down.

It’s way easier to focus and sleep.

In short, white noise is putting your brain in some short of dampened mental state, and therefore it’s easier to focus or sleep. And for the ones that are craving for sleep or lack focus, be sure to check out the ultimate 10 hour white noise video below! (Or, just yank out the coax cable from your TV set, it might do just as well.)

Watch the video. URL: https://youtu.be/bNqERBWaJeM

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Smokers Feel More Pain


Compared with patients with no tobacco smoke exposure, smokers needed 38% more propofol to induce anesthesia, and passive smokers needed 18% more, reported lead investigator Erdogan Ozturk, MD, of Bezmialem Vakif University in Istanbul, and colleagues.

“A limited number of studies exist indicating that smoking increases anesthetic requirements; however, anesthetic agent requirements for individuals exposed to environmental tobacco smoke (passive smokers) have not been studied at all,” the investigators wrote.

Ninety women undergoing total abdominal hysterectomy were enrolled in the study. They were divided into three groups of 30 each based on smoking status: smokers, passive smokers, and nonsmokers. (Nonsmokers had no history of smoking or environmental tobacco smoke exposure).

Smoking status was confirmed by measuring serum cotinine, a metabolite of nicotine and marker of tobacco smoke exposure.

Standard total intravenous anesthesia was performed on all patients. Bispectral index values were maintained at 40-60. After each operation, the investigators assessed the total amounts of propofol and the painkiller remifentanil used.

The average amount of propofol used to induce anesthesia was 102.76 mg for smokers, 84.53 mg for passive smokers, and 63.17 mg for nonsmokers. Smokers needed 38% more propofol than nonsmokers and 17% more than passive smokers to induce anesthesia. Passive smokers needed 18% more propofol than nonsmokers. (P<0.05 for all.)

Total propofol usage for the entire procedure was 179.38 mg for smokers, 150.50 mg for passive smokers, and 119.37 mg for nonsmokers. Smokers used 33% more anesthesia than nonsmokers and 16% more than passive smokers. Passive smokers used 20% more anesthesia than nonsmokers. (P<0.05 for all.)

Total amounts of remifentanil used were 1,315 mcg for smokers, 1,241 mcg for passive smokers, and 1,010 mcg for nonsmokers. Smokers used 23% more of this painkiller than nonsmokers and 6% more than passive smokers. Passive smokers used 18% more than nonsmokers. (P<0.05 for smokers versus nonsmokers.)

“We concluded that the amount of the anesthetic and analgesic required to ensure equal anesthetic depth in similar surgeries was higher in active smokers and passive smokers compared to nonsmokers,” the researchers concluded.

One potential explanation for the results is that nicotine affects the metabolism of anesthetic drugs in the liver. “Our starting point was the idea that cigarettes, which contain more than 4,000 chemicals, may affect drug metabolism,” Ozturk told MedPage Today via email.

“I suggest that healthcare professionals should consider the effect of smoking in their research and plan customized treatment options for each individual. This will optimize the medication process and contribute to the reduction of health expenditures,” Ozturk said.

Because so few studies have explored the question, anesthesiologists generally aren’t aware that smokers may need more anesthesia during surgery, Richard Dutton, MD, an anesthesiologist at the University of Chicago and Chief Quality Officer for the American Society of Anesthesiologists, said in an interview with MedPage Today. Dutton was not involved in the study.

“This is a surprise,” Dutton said. “It’s not something I would have predicted, but I am inclined to believe the results. I would love to see it replicated in a larger study population.”

“It’s biologically plausible. Cigarette smoke is a brain stimulant, and a patient on stimulants needs more anesthesia to get to sleep,” Dutton said.

There is normally 10% to 20% individual variation in the amount of anesthesia patients require, so the 38% difference between smokers and nonsmokers for inducing anesthesia is substantial, Dutton said.

In addition, the fact that smoking status was objectively ascertained by measuring cotinine, rather than relying on self-reports, is an important strength of the study Dutton said.

“If this is borne out by other studies, it could affect clinical practice,” Dutton said. “We should probably be aware that smokers might require more anesthesia.”

Dinosaur blood cells extracted from 75-million-year-old fossil .


Jurassic Park saw dinosaurs brought back to life based on DNA preserved in the gut of a blood-sucking mosquito entombed in amber. Now we have found what appears to be real dinosaur blood inside a bog-standard fossil bone.

“We stumbled on these things completely by chance,” says Susannah Maidment of Imperial College London, whose team was trying to study bone fossilisation by cutting out tiny fragments of fossils.

Instead, they found blood-like cells and collagen from 75-million-year-old dinosaur fossils – 10 million years before T. rex appeared.

Although the cells are unlikely to contain DNA, those extracted from better preserved fossils using the same technique may do so, she says.

And even without DNA, soft tissue cells and molecules could help us learn much more about dinosaur physiology and behaviour, the team says. For example, the physical size of blood cells can reveal insights into metabolism, and the possible transition from a cold to warm-blooded existence.

So far, such soft flesh tissues were only ever found in serendipitous fossils preserved in exceptionally rare circumstances, for example, by being frozen in ice or in a dry environment free of microbes that would otherwise break down the flesh, says Maidment.

Blood cells came from this claw

“But the fossils we looked at were not rare at all,” she says. They were ordinary bones collected from the surface at the well-known Dinosaur Park Formation in Canada.

To study fossil bones, the team borrowed a medical research technique based on a focussed ion beam, that is giving clues to how blood vessels become calcified and cause heart attacks. Their intention was to study how natural bone minerals fossilise, and what happens when collagen decays in dinosaur bones.

“This beam works like a knife, with a microscopic robotic arm bearing a needle that enables you to cut out fragments of interest,” says Sergio Bertazzo, also of Imperial College London, who co-led the investigation.

Bird-like collagen fibres

Three-dimensional examinations of the blood-like cells under an electron microscope revealed that they had nuclei, so human red blood cells could not have contaminated the sample, because they have no nuclei.

And when Maidment analysed the chemical composition of the red blood cells with a technique called mass spectrometry, the spectrum was surprisingly similar to that of blood taken from a living bird, an emu, adding further evidence to it being from a dinosaur.

Maidment is now hoping to investigate more samples. “We want to understand how this preservation can occur, how far back in time it happens, and what type of rock it happens in,” she says.

The discovery was welcomed by John Asara of Harvard Medical School, whose team reported in 2007 finding collagen in a 68-million-year old T. rex and in an 80-million-year old brachylophosaurus fossil. Asara says this field of science has been barely tapped.

“Papers like this do much to advance the field, by showing that fossils are more than ‘just rocks’, and opening the door to the possibility that materials persist in ancient fossils that were not thought possible only a few years ago,” says Mary Schweitzer of North Carolina State University in Raleigh, who reported extracting blood from T. rex in 2009. “[It also] seems to indicate, like our own findings, that this is not necessarily an exceedingly rare occurrence.”

A genetic link has been found between mental illness and creativity.


Mental illnesses such as schizophrenia and bipolar disorder may share some genetic roots with creativity, new research suggests.

After looking at genetic data taken from more than 150,000 people, researchers have found that those in artistic and creative careers are more likely to carry genes that predispose them to a risk of mental illness than non-creative professionals. But the study, which is published in Nature Neuroscience, has been met with plenty of healthy scepticism, not least of all due to the researchers’ definition of ‘creativity’.

 

This isn’t the first time that a genetic link between mental illness and creativity has been suggested. Historically, many of society’s most brilliant minds also struggled with mental issues, helping to enforce the stereotype of the ‘tortured artist’, and arange of studies over the years has also helped to support the link. However, genetic evidence has been pretty patchy up until now.

In the new research, a team of scientists from biopharmaceutical company deCODE genetics in Iceland looked at data taken from 86,000 Icelandic people.

They found that individuals who worked in an artistic profession or who belonged to a national artistic society were 17 percent more likely to carry genetic variants linked to bipolar disorder or schizophrenia than other members of the public.

The team then replicated their research with data taken from people in the Netherlands and Sweden, and found that, in this subset, creatives were nearly 25 percent more likely to carry the mental disorder genes than their non-creative peers.

“This could not be accounted for by increased relatedness between creative individuals and those with psychoses, indicating that creativity and psychosis share genetic roots,” the authors write in Nature Neuroscience.

But critics of the study now question whether we can really classify someone as creative simply by their profession, and whether the genetic links found are all that significant, as Arielle Duhaime-Ross writes for The Verge:

“But here’s the thing: the increase in risk can be kind of misleading. Together, the variants used the study only explain about 6 percent of schizophrenia and 1 percent of bipolar disorder, according to a graph in the study. And these same variants only explain about one-quarter of 1 percent of artistic ability.”

In other words, the genes that predict risk of mental illness might help make people a tiny bit more creative, but something else – whether genes or environmental factors – must be involved to get them the rest of the way.

“There is a link, and it is astonishingly weak in the sense that most people would care about,” population geneticist David Culter from Emory University in the US, who wasn’t involved in the study, told Duhaime-Ross.

However, CEO of deCODE Kari Stefansson hopes that the results will help put mental illness in a positive light for once.

“To be creative, you have to think differently,” Stefansson told Ian Sample over at the Guardian. “And when we are different, we have a tendency to be labelled strange, crazy and even insane.”

Doctors remove 420 kidney stones ’caused by excessive tofu’ from patient in China .


Doctors in China have removed 420 kidney stones from a man’s body, blaming an excessive amount of tofu in his daily diet.

Mr He from Zhejiang Province in eastern China, checked into the Dongyang People’s Hospital complaining of intense pain in his abdomen last month. A CT scan revealed that his left kidney was packed full of stones, most of them tiny.

The stones removed by doctors

Doctors operated on Friday in an agonising procedure that lasted about two hours.

Mr He said he had a history of suffering from kidney stones. Twenty years ago he had 10 stones removed using a procedure called lithotripsy, which sends shock waves to break up stones in the kidney, bladder, or ureter until they are small enough to pass in the urine.

“I have worked as a doctor for 30 years and have never seen so many stones,” said Zhou Changchun, the attending surgeon, according to state newspaper Qianjiang Evening Post.

The unusually high number of stones was attributed to the high concentration of gypsum tofu, a popular local food, in Mr He’s diet. The tofu contains calcium sulphate, which cannot be expelled from the body without a sufficient intake of water.

Wei Yubin, the chief surgeon, said that the kidney would have stopped working had Mr He delayed seeking medical attention any longer, and the kidney most likely removed.


The stones removed by doctors (EuroPics)

This time, the doctors used forceps to remove each stone one by one.

“We spent 45 minutes just taking out the tiny stones,” said Dr Wei. “After the operation, my hands and legs were both numb.”

Following the operation, Mr He took his stones home with him in a plastic bag.

The medical name for kidney stones is nephrolithiasis. If the stones cause severe pain, this is known as renal colic. Most kidney stones are small enough, between 4 to 5mm in diameter, to be passed naturally.

Kidney stones are quite common and usually affect people aged 30 to 60 years. It is estimated that renal colic affects about 10 to 20 per cent of men and three to five per cent of women, according to the NHS.